steve777
Member
there are known side effects with IGF-1. IMO these are amplified with longR3 because long R3 will not bind to endogeous binding proteins. these binding proteins serve to protect certain tissues from the actions of IGF-1 while simultaneously delivering IGF-1 to the necessary target tissues (where locally acting proteases will free up the IGF-1)
longR3-IGF-1 is IGF-1 running rampant in the body. This is troublesome
I think longR3 might be useful for connective tissue injuries (direct injection) but for other uses the risk to benefit ratio is too high
when explained this way, longR3-IGF-1 IS scary regarding "unprotected" tissues throughout the body. Perhaps there is a "safer" way to get the desired effect by changing the number of naturally occuring proteases present in muscle to enhance the effect of the IGF-1 already present? Could the proteases present in muscle be the limiting factor in unlocking the process or has science determined the limiting factor is the amount of IGF-1 being produced?